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==Description==
==Description==
Clastridiurre perfringens type A causes
enterotoxemia, or yellow lamb disease,
which occurs primarily in the western US
(McGowan et al., 1958). Depression, anemia,
icterus and hemoglobinuria, are followed
by death after a clinical course of
6-12 h, and large numbers of C. perfringen.
s are found in intestinal contents. A
similar condition occurs in goats (Russell,
1970), and type A probably also causes
tympany, sometimes accompanied by
hemorrhagic, necrotic abomasitis in calves.
Gram-positive bacilli are demonstrable on
the mucosa and in the submucosa and a
toxin is found in intestinal contents
(Roeder et al., 1988). Intravascular hemolysis,
capillary endothelial damage, platelet
aggregation, shock and cardiac effects in
natural infections are predictable systemic
actions of a hemolytic toxin (Stevens et
al., 1988; Timoney et a]., 1988). Chymotrypsin
resistance of a toxin from
enterotoxemia isolates may allow accumulation
in the gut and entry to circulation
(Ginter et al., 1995).
C. pgheernfrsi type B is frequently isolated
from cases of dysentery in newborn
lambs (table II) and hemorrhagic enteritis
in goats (Frank, 1956). Disease is more
common in the UK, South Africa and the
Middle East than in the US (Timoney et
al., 1988). In lambs, inappetence, abdominal
pain and bloody diarrhea are followed
by recumbency and coma. Lesions consist
primarily of hemorrhagic enteritis,
with evidence of enterotoxemia (Frank,
1956). Chronic disease in older lambs
(’pine’) is characterized by chronic
abdominal pain without diarrhea. Pathogenesis
of type B infections may be due to
additive or synergistic effects of a, p and
c toxins.
Neonates of most species are highly
susceptible to infection by C. perfringen.s
type C (MacKinnon, 1989) (table ll), and
colonization in advance of normal intestinal
flora or alteration of flora by dietary
changes are significant factors in pathogenesis
(Timoney et al., 1988). In lambs,
type C infection resembles lamb dysentery,
and may be accompanied by nervous
signs, including tetany and opisthotonus.
Peracute death, occasionally without other
clinical signs, is not uncommon, but the
clinical course may also extend to several
days. Young ewes and other adult sheep
can also develop type C enterotoxemia, a
condition known as ’struck’, in which the
clinical disease occurs so rapidly that it
often suggests that the animal has been
struck by lightning. Mucosal damage, perhaps
caused by poor quality feed, facilitates
abomasal and small intestinal multiplication
of organisms, with resulting
mucosal necrosis. Fluid accumulation in
the peritoneum and thoracic cavity suggest
toxemia, and enteric lesions, dysentery
and diarrhea are often absent (Sterne
and Thomson, 1963). Similarities of cpb,
the (3 toxin gene, to the genes for staphylococcal
a and y toxins and leukocidin
(Hunter et al., 1993), strengthen suggestions
that (3 toxin may affect the CNS
(Jolivet-Reynaud et al., 1986; McDonel,
1986). However, hemorrhagic enterotoxemia
has not been reproduced in lambs by
inoculation with cell-free culture supernatant
fluid (Niilo, 1986).
Enterotoxemia (’overeating’) in sheep
of all ages except newborns is caused by
C. perfrivgetes type D (table II) (Timoney
et al., 1988). Lambs 3-10 weeks old, suckling
heavily lactating ewes, are commonly
affected, as are feedlot animals up to 100
months of age. Upsets in the gut flora, following
sudden changes to a rich diet, continuous
feeding of concentrates (Popoff,
1984), and the presence of excess dietary
starch in the small intestine are often
involved. e toxin facilitates its own absorption
(Niilo, 1993), resulting in toxemia
with little or no enteritis. Some animals
display dullness, retraction of the head,
opisthotonus and convulsions (Niilo, 1993;
Popoff, 1984), but sudden death is common.
Degeneration and necrosis in the
CNS is typical (Buxton and Morgan,
1976), and focal encephalomalacia is a
chronic neurological manifestation of nonfatal
disease (Griner, 1961; Buxton and
Morgan, 1976). The extent of incoordination
and convulsions is directly related to
the severity of lesions (Griner, 1961). Peritoneal
and pericardial effusions are typical
in sheep, and glycosuria is pathognomonic
(Gardner, 1973; Niilo, 1993). The common
name ’pulpy kidney’ derives from
the post mortem autolysis of hyperemic,
toxin-damaged tissue.
Goats develop catarrhal, fibrinous, or
hemorrhagic enterocolitis. The condition
is often chronic, and pulpy kidney is
absent (von Rotz et al., 1984; Blackwell
and Butler, 1992).
C. perfringens type E is an apparently
uncommon cause of enterotoxemia of
lambs (table II), and recent isolates have
been obtained from calves with hemorrhagic
enteritis, in the western and midwestern
US (Meer and Songer, 1997).
However, type E remains of uncertain
overall importance in animal disease.
An increasing body of evidence suggests
a role for enterotoxigenic strains,
particularly of type A, in the etiology of
diarrheal conditions in several animal
species (Estrada-Correa and Taylor, 1989;
Niilo, 1993). In one study, CPE production
was observed in 12 % of isolates from cattle,
sheep and chickens with enteritis
(Niilo, 1978), and in another, genotyping
revealed that about 5 % of isolates are
enterotoxigenic, with most of these being
type A (Songer and Meer, 1996; Meer and
Songer, 1997).
CPE is weakly immunogenic when
administered via the intestinal tract. Disease
gives rise to serum antibodies in
sheep and other domestic species, but antibodies
produced following parenteral inoculation
are not protective (Niilo and Cho,
1985; Estrada-Correa and Taylor, 1989).
The best target for immunoprophylaxis
may be the toxin’s membrane binding
event (Hanna et al., 1989; Mietzner et al.,
1992).
Immunoprophylaxis is a control measure
of paramount importance, due to the
rapid and frequently fatal course of disease
caused by the various types of C. perfringens.
Lambs born to ewes vaccinated
against types B, C or D are protected
against dysentery (Smith and Matsuoka,
1959; Kennedy et al., 1977; Odendaal et
al., 1989), and may be immunized at 3
days of age (Kennedy et al., 1977). Enterocolitis,
but not toxemia, may occur in
vaccinated goats (Blackwell et al., 1991;
Blackwell and Butler, 1992).
Infection with Clostridium perfringens types B and C causes severe enteritis, dysentery, toxemia, and high mortality in young lambs, calves, pigs, and foals. Types B and C both produce the highly necrotizing and lethal β toxin that is responsible for severe intestinal damage. This toxin is sensitive to proteolytic enzymes, and disease is associated with inhibition of proteolysis in the intestine. Sow colostrum, which contains a trypsin inhibitor, has been suggested as a factor in the susceptibility of young piglets. Type C also causes enterotoxemia in adult cattle, sheep, and goats. The diseases are listed below, categorized as to cause and host. C perfringens also has been associated with hemorrhagic enteritis in dogs. (See also intestinal diseases in horses, Intestinal Diseases in Horses and Foals: Introduction.)
Infection with Clostridium perfringens types B and C causes severe enteritis, dysentery, toxemia, and high mortality in young lambs, calves, pigs, and foals. Types B and C both produce the highly necrotizing and lethal β toxin that is responsible for severe intestinal damage. This toxin is sensitive to proteolytic enzymes, and disease is associated with inhibition of proteolysis in the intestine. Sow colostrum, which contains a trypsin inhibitor, has been suggested as a factor in the susceptibility of young piglets. Type C also causes enterotoxemia in adult cattle, sheep, and goats. The diseases are listed below, categorized as to cause and host. C perfringens also has been associated with hemorrhagic enteritis in dogs. (See also intestinal diseases in horses, Intestinal Diseases in Horses and Foals: Introduction.)